GSK ends Alector neuroscience deal after trial failures
GSK has pulled out of its neuroscience collaboration with Alector, ending a 2021 alliance that began with a $700m upfront payment but has since been hit by two clinical setbacks.
Why it matters: The move is another reminder of how difficult neurodegeneration remains for big pharma, even as Alzheimer’s and dementia research attracts renewed investment after the first disease-modifying amyloid drugs reached the market.
Backstory: GSK and Alector partnered on two progranulin-targeting antibodies: latozinemab, also known as AL001, and nivisnebart, also known as AL101.
- The original agreement gave Alector $700m upfront and left it eligible for up to $1.5bn in further development-related milestones, plus royalties.
Zoom in: Latozinemab was being developed for frontotemporal dementia caused by progranulin gene mutations, a rare inherited form of the disease.
- The phase 3 INFRONT-3 study failed to slow disease progression, prompting Alector to remove the programme from its pipeline and cut nearly half its workforce.
The second blow: Nivisnebart, which was being tested in Alzheimer’s disease, was discontinued after an interim analysis showed the phase 2 INVOKE-2 trial was unlikely to meet its primary endpoint.
How it works: Both drugs were designed to increase progranulin, a protein involved in lysosomal function and neuroinflammation. The biology remains scientifically attractive, but the clinical readouts have not yet translated into convincing efficacy.
Yes, but: The termination does not necessarily close the door on progranulin biology. It does, however, remove GSK’s support from Alector’s most prominent partnered neuroscience programmes and leaves the biotech with a significantly narrower clinical-stage story.
The bottom line: GSK is cutting its losses on a once high-profile dementia alliance, while Alector is left to rebuild after two failed attempts to turn progranulin modulation into a clinical win.
